Download A simple method of weighing the heart

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project

Document related concepts

Cardiovascular disease wikipedia , lookup

Electrocardiography wikipedia , lookup

Quantium Medical Cardiac Output wikipedia , lookup

Heart failure wikipedia , lookup

Myocardial infarction wikipedia , lookup

Lutembacher's syndrome wikipedia , lookup

Coronary artery disease wikipedia , lookup

Cardiac surgery wikipedia , lookup

Mitral insufficiency wikipedia , lookup

Antihypertensive drug wikipedia , lookup

Arrhythmogenic right ventricular dysplasia wikipedia , lookup

Atrial septal defect wikipedia , lookup

Dextro-Transposition of the great arteries wikipedia , lookup

Transcript
Downloaded from http://jcp.bmj.com/ on May 10, 2017 - Published by group.bmj.com
J. clin. Path. (1961), 14, 578
A simple method of weighing the heart
A. G. MARSHALL
From The Royal Hospital, Wolverhampton
A simple method of dividing and weighing the heart is described. It is quick to perform
and ratios between the left and right ventricles and the total weight of the heart are remarkably
SYNOPSIS
constant.
Analysis of 788 cases shows that these ratios are of value in the diagnosis after death of systemic
and pulmonary hypertension. This is applicable to both sexes at all ages.
An unexpected finding was a significant correlation between pulmonary hypertension and acute
massive pulmonary embolism, of which the prophylactic and therapeutic implications are mentioned.
The value of the method in childhood and infancy is indicated.
Weighing the heart is a usual procedure in routine
necropsies but its value is restricted in any particular
case by ignorance of the normal weight and by the
difficulty of determining the contribution of each
part of the heart to a variation from the supposed
normal. A method of dividing the organ in order to
weigh its various parts was described by Lewis (1914)
but the procedure takes some weeks to complete and
this limits its value in routine work. Some pathologists estimate hypertrophy of the ventricles by
measuring the thickness of their walls but in our
hands this has not been successful owing to the
irregularity of the endocardial surfaces. Others
assess the presence of pulmonary hypertension by
measurements of the pulmonary vessels in histological sections (Heath and Whitaker, 1955) but we
have found this unsatisfactory for routine work.
Some years ago a standard technique for dividing
and weighing the heart was adopted, and having
collected data from 788 cases the findings are presented here in the hope that the method will be
useful to others. The technique was purposely made
as simple as possible as time is often limited in
routine work and great accuracy was deliberately
sacrificed for the same reason. The whole procedure
takes only a few minutes and results in fairly comparable figures. The whole of the interventricular
septum is weighed with the left ventricle and no
attempt is made to separate the two auricles; the
pericardial fat and coronary vessels are not removed
from the surface of the heart. It was intended to
avoid defining the weight of the normal heart by
Received for publication 13 July 1960.
578
calculating the ratios of the weights of its various
parts.
METHOD
Although Lewis (1914) explains his method at length,
Herrmann and Wilson (1922) found that his directions
were not explicit enough to prevent misunderstanding.
Our technique is therefore set out below in full detail of
each step we actually take and illustrated in Figs. 1 to 3.
1 The thoracic contents are removed in toto and the
heart is not removed from them until step 7 below.
Running water is used when required throughout the
examination.
2 After examining the remainder of these organs and
opening the pericardium to its apex, the right auricle is
opened with scissors and examined with the tricuspid
valve.
3 A long knife is then passed through the tricuspid
orifice to the apex of the right ventricle and this is
opened by an incision along the length of its extreme
outer border.
4 With scissors laid flat against the right ventricular
surface of the interventricular septum, the right ventricle
is cut off it from apex to base along its anterior junction
with it. None of the right ventricle now remains attached
anteriorly to the septum, and the incision is continued
through the pulmonary valve and into the pulmonary
artery and its branches (Fig. 1).
5 Having examined the right chambers, steps 2 and
3 are now copied exactly on the left side thus exposing
the left auricle, mitral valve, and most of the left ventricle.
6 The aortic valve and thoracic aorta are now opened
by cutting upwards through the mitral valve and the
aortic valve with scissors.
7 The heart is now removed from the other viscera
by lifting it vertically, apex upwards, with the remainder
Downloaded from http://jcp.bmj.com/ on May 10, 2017 - Published by group.bmj.com
A simple method of weighing the heart
579
of the thoracic viscera hanging from it. The pulmonary
veins and venae cavae are now divided at their junctions
with the auricles, and the aorta and pulmonary arteries
are divided at the level of the upper edges of their valve
cusps. It is most important that these vessels be divided
at these respective levels and we draw attention to the
possibility of error at this stage (Fig. 2).
8 All the remaining blood clot is washed away and
lightly adherent thrombus removed with forceps. The
heart is now weighed.
9 The coronary arteries are now opened and examined
as may be desired.
10 The posterior attachment of the right ventricle to
the septum is now divided, again with scissors laid flat
against the right ventricular surface of the septum.
4
FIG. 1. Cutting the right ventricle from the right side of
the septum anteriorly.
FIG. 3. The heart as finally divided. Above, the auricles;
below on the left, the left ventricle; below on the right, the
right ventricle in its two parts.
2. Removing the heart from the other thoracic
viscera. Note the manner in which the anterior edge of the
right ventricle has been cut from its junction with the
FIG.
septum.
11 The auricles are now removed by cutting them off
the ventricles or pieces of ventricle along the coronary
sulcus, and joining these incisions across the top of the
septum. The heart is thus divided into four pieces (a) the
auricles, (b) the left ventricle attached to the septum, and
(c) the right ventricle in two pieces. The two ventricles
are weighed, recording (b) as the left ventricle and (c) as
the right (Fig. 3). Simple ratios are calculated as follows
to one place of decimals.
Weight of left ventricle
L/R
Weight of right ventricle
Weight of whole heart _ T/R
R
Weight of right ventricle
Downloaded from http://jcp.bmj.com/ on May 10, 2017 - Published by group.bmj.com
A. G. Marshall
580
Weight of whole heart
T/L
Weight of left ventricle
The weight of the auricles can be determined by subtraction.
RESULTS
The material available consists of the data from 788
post-mortem examinations, being all the routine
necropsies performed at one hospital in the years
1954-57, except for a small number which had to be
discarded on the grounds of insufficient information.
There are 650 adults (429 of them males), 20 adolescents aged 10 to 20 years, 23 children aged 1 to 10
years, and 95 infants under 1 year of age. Most of
the discards were infants whose hearts had not been
divided.
Our attention was first directed to adults and the
findings were considered for each sex in age groups.
As usual in routine hospital work there is a preponderance of cases in the sixth and seventh decades.
The numbers in the younger age groups from which
it might be expected to discover the normal values
are small but from them and from accident cases
ideas were formed as to the probable directions in
which deviations might be expected to occur. It
became necessary to place an arbitrary maximum
for the weight of the normal heart in each sex in
order to determine the approximate normal values
for the new measurements. There is no real agreement on the maximum weight of the human heart
(Zeek, 1942) and it has been the custom for many
years in our department to regard it as 350 g. for
males and 300 g. for females. As we have no facilities
for weighing the bodies (Bartels and Smith, 1932),
these figures were taken as normal and have proved
satisfactory. Indeed, raising the values to 400 g. and
350 g. respectively did not greatly affect the overall
results but did include a number of clinically
abnormal hearts in the normal groups.
DISTRIBUTION OF HEART VVEIGHTS At this point it
seems worth while to examine the distribution of
heart weights in this material. Largely on the basis
of the clinical history in each case and with due
regard to the general post-mortem findings, all the
adult hearts (20 years and above) were divided into
three populations.
1 No vascular disease or normal This refers in
fact to the absence of systemic hypertension or
chronic pulmonary disease (see 3 below), and includes
conditions other than hypertension which might
give rise to cardiac hypertrophy, e.g., aortic valvular
stenosis, pericarditis, etc.
2 Systemic hypertension A clinical history consistent with it and blood pressure above 140/90 mm.
Hg.
3 Pulmonary disease excluding hypostatic pneumonia or single attack of lobar pneumonia Conditions which might reasonably be expected to give
rise to pulmonary hypertension such as mitral
stenosis were included. When systemic hypertension
was also present, the case was placed in group 2.
Figure 4 shows the distribution of total heart
weights in these three classes. There is some tendency
to support our arbitrary estimate of normal heart
weight, since in males the hearts of only eight
(3 5 %) of cases of systemic hypertension fall below
350 g. and in females only five (5-5 %) fall below
300 g. It is possible that in some of these patients a
sufficient degree of cardiac hypertrophy had not
been achieved to bring the heart weight above these
values. It is admitted that in each sex roughly one
third of the 'normals' is found above these weights
but these, of course, include hearts enlarged for
some reason other than hypertension and those
where there was insufficient evidence for a firm
diagnosis of hypertensive disease. In both sexes the
cases of pulmonary disease are fairly evenly distributed throughout the range; total heart weight is
little help in the diagnosis of pulmonary hypertension.
In normal hearts the weight of the right ventricle
by our method is about 80 to 100 g. and the left
ventricle weighs about 100 g. more. In females these
figures are smaller by some 20 g. The weight of the
auricles was more variable and we have failed
to attach any significance to these variations. In
normal hearts of whatever weight and in both sexes
the ratios were remarkably constant as follows:
L/R 2 to 3, T/R 3 to 5, and T/L 15 to 2.
In left ventricular hypertrophy it would be
expected that the first two ratios would become
larger and the last smaller. In known cases of
systemic hypertension or aortic valvular disease
L/R and T/R were found to be increased beyond
3 and 5 respectively, though in some cases only one
was raised. It seemed therefore that when L/R equals
or exceeds 3 and/or T/R equals or exceeds 5 (values
'raised' or 'increased') there is left ventricular hypertrophy associated with systemic hypertension unless
some other explanation can be found.
Lewis (1914) remarks that the commonest type of
cardiac hypertrophy is a uniform hypertrophy and
in this case these ratios could be either normal or
increased.
In the conditions which are usually associated
with pulmonary hypertension such as mitral stenosis,
Fallot's tetralogy, and pulmonary fibrosis the ratio
T/L is greater than L/R or equal to it ('ratios reversed') and this was the case in 58 % of infants
mostly in the first few days of life (Table IV). Such a
deviation would be expected in right ventricular
~ ~b
Downloaded from http://jcp.bmj.com/ on May 10, 2017 - Published by group.bmj.com
A simple method of weighing the heart
581
oW
w
_0
00C
>
I-,
z
0
'bbo
W z
f)
)w
wa:r
W w
IEEMN,E
a- :.
Li
0)
-
so
'b
U,
Uo
0
_!
i
Oa -
_~~~
_
th
n
o
8°'
6
0
in
U1
in
in
_!
0
b
LL
in
UN
b
I0h
LA
tn
Ln
_
N
0
'0
U,
Un
M> 0
z
OU) Z
I,
:z
in
n>0
'0
I-
0
0
U,
N
b
MM
Un
in
Uq
0
in
0
N
in
N
in
1
0
0
WEIMMEXIMMI'm
N
It
I
in
0
1
1
I
I
r,
2
in
tI
1
__m
0
In
Iffil
'Ww"I'MMISMEMIM
ii)
I
In
N
in
C')
I
N
0
0
in
0
U'
Nk
C uJ
cr
0
NIL4
L In'
N
in
N19
U'
NL
0
0
In
U I
---=I
3:
8
eq
0
N O
'
)
mcn
()
C
;0
NN
N-O
_
_
_
0
N
tN
N
S3SVZ
30
b3SW4lN
N O
O
<
o
I-
I-C
'a
N
0
N
m
la
v
S3SVS
N
00
i0
la
kf3gv4nN
N
Downloaded from http://jcp.bmj.com/ on May 10, 2017 - Published by group.bmj.com
582
A.
G.
Marshall
hypertrophy and it was therefore concluded that it
indicates pulmonary hypertension if other explanations are lacking.
In order to test the validity of these two conclusions the adult cases were divided first into two
main categories, those with normal and those with
increased heart weights using the arbitrary standards.
Each category was subdivided into three groups,
namely, (a) ratios normal L/R<3, T/R<5, and
T/L<L/R; (b) ratios raised L/R>3, and/or T/R.5,
T/L<L/R; (c) ratios reversed T/L.L/R (D<O).
The 788 cases were allocated to these groups in
the three categories as defined above, those having no
vascular disease, those having clinical systemic hypertension, and those dying of pulmonary disease
excluding terminal or hypostatic pneumonia. The
few cases of mitral stenosis or Fallot's tetralogy
were included as pulmonary disease. Being puzzled
as to the place of acute pulmonary embolism, such
cases were at first placed in a separate category. The
tabulated results for the two sexes in three age groups
are shown in Table I. The results of simple significance tests on these figures are also shown and they
tend to confirm our conclusions that 'raised' values
of L/R and/or T/R are associated with systemic
hypertension while 'ratios reversed' in which D
(L/R-T/L) is 0 or less than 0 are associated with
pulmonary hypertension. The ratios L/R, T/R, and
for D (L/R-T/L) were therefore analysed further
as shown in Figs. 5, 6, and 7. It can be seen that
(1) L/R is 3 or more in only 25 (15%) of males
and in 15 (14%) of females with no hypertensive
TABLE I
CLASSIFIED RESULTS IN ADULTS AND NUMBER OF CASES IN EACH CATEGORY
20 to 49 Years
Male
T. normal
Ratios
normal
T. normal
Ratios
raised
No vascular disease" 29 (88)
Systemic hypertension"
0
Pulmonary disease' 3 (9)
Pulmonary embolism 1 (3)
Total
33
Ratios
reversed
T. raised
Ratios
normal
T. raised
Ratios
raised
T. raised
Ratios
reversed
70 Years and Over
Female
Total
Male
Female
24 (100)
53 (94)
49 (74-5)
15 (68-1) 64 (73)
0
0
0
0
24
3 (4-5) 0
3 (5-2) 13 (195) S (22-8)
1
(1-8) (66
S) 2 (9-1)
57
66
22
Total
Male
3 (3-4)
18 (20-2)
3 (3-4)
5 (62 5)
22 (73-2)
1 (12-5)
0
2
8
2 (6-7)
4 (13-4)
2 (6-7)
30
0
22
(25)
6 (66 7)
10 (62-5)
5
(50)
15 (57-7)
5 (50)
3 (60)
(33-3)
4 (25)
2 (12-5)
0
16
5 (50)
0
7
3
0
0
9
9 (34-6)
2 (7-7)
0
26
4 (40)
1 (10)
0
10.
2 (40)
0
0
No vascular disease 0
Systemic hypertension
0
Pulmonary disease 3 (100)
Pulmonary embolism 0
Total
3
0
0
0
2 (100)
No vascular disease S (18-5)
Systemic hypertension
22 (81-5)
Pulmonary disease 0
Pulmonary embolism 0
Total
27
2
No vascular disease 2 (14-3)
Systemic hyper12 (85-7)
tension
Pulmonary disease 0
Pulmonary embolism 0
Total
14
No vascular disease 3 (25)
Systemic hyper-
tension
0
Pulmonary disease 9 (75)
Pulmonary embolism 0
Total
12
0
0
10
1 (8-3)
2 (22-2)
3 (14-2)
0
5 (100)
0
5
0
10 (83-4)
1 (8 3)
12
0
2 (22-2)
0
12 (57-4)
6 (28-4)
21
0
4 (66-6)
1 (16-7)
6
5 (50)
10 (27-1)
17 (26-2)
4
(12-5)
21 (21-6)
4 (16-6)
3 (30)
1 (10)
1 (10)
10
25 (67-6)
1 (2-7)
1 (2-7)
37
32 (49-2) 20 (62-5)
10 (15-4) 2 (6-3)
6 (9-2) 6 (18-7)
65
32
52 (53-6)
12 (12-4)
12 (12-4)
97
16 (66-8)
0
2
2 (9-4)
0
2
(5-2)
17 (81-2)
2 (9-4)
0
21
33 (84-5)
3 (7-7)
1 (2-6)
39
2 (20)
5 (22-7)
0
7 (70)
1 (10)
10
0
16 (72-8)
1
22
5 (71-4)
2 (28-6)
0
7
5 (556)
9
1
(5-5)
3
18
48 (84-2)
4 (7-0)
2 (3-5)
57
7 (20)
3 (37-5)
10
0
26 (74-3)
0
3 (37-5)
2 (25)
8
0
29 (67-5)
4 (9-3)
43
(4-5) 352 (5-7)
1
(16-7)
2 (8-3)
2 (8-3)
24
(5-3)
15 (83-5)
1 (5-5)
1 (5-5)
8
(25-8)
20 (64-6)
2 (6-4)
1 (3-2)
31
(23-2)
4
(33-3)
1 (8-4)
5 (41-6)
2 (16-7)
12
-
>
8
(53-4)
139 (79-5)
5
(58)
S
3 (100)
4 (44-5)
7 (20)
0
0
0
4 (44-5)
1 (11)
9
0
21 (60)
7 (20)
35
0
3
(6-6)
107 (60-1)
8 (16-4)
13 (10-4)
3
(37-5)
0
2 (25)
3
8
(3-5)
38
15
(21-4)
(8-4)
18 (10-1)
178
2
12 (34-4)
1 (2-8)
Xs} 22 (42-8)}(621
35
41 (23)
108 (60-7)
1129 (6*2))(16,3
(10-1)
18*
1
178
13 (10-2)
36 (73-4) 101 (79-4) 102 (80-4)
2 (4-1)
8 (6-3)
7} 12 (g
3 (6-1)
5 (3-9)
49
127
127
7
(35)
1 (5)
7 (35)
(37-5) 205 (25)
(25-8)
24 (28-2)
1 (1-2)
1 (1-2)
21
52 (61-2)
10 (11-8)
85
(8
29 (58)
50
7 (15-9)
0
14
50
30 (68-2)
2
5 (11-4)
44
16 (88-9)
0
2 (11-1)
18
6f
175
19 (38)
2
(4)
(15)
(4-5)
6 (3-5)
'
(45
18 (36)
3 (6)
14 (70)
0
3(15)
20
3
155 (88-5)
(14-2)
25
6 (3-4)
175
29
Grand Total aft,, R,
allocation of Q.,Il
Carcinoma of it,,-.1
(2-9)
6 (40)
1
0
15
Figures in brackets denotes percentages
Association between increased heart weight and raised ratios L/R and TjR or reversed ratio D (L/R T/L)
'No vascular disease, both
0-145
0-8
P > 0-7
N.S.
X'
sSystemic hypertension, both sexes x' = 4-72 0-05 > P > 0-02 S.
'Pulmonary diseases (pulmonary embolism included), both sexes x' = 0-001 0-95 > P > 0-90 doubtful significance
sexes
Total
1 (4-5)
2 (28-6)
0
Grand
-Total
17 (77-5)
4(18)
8.8
Female
5 (71-4)
No vascular disease 1 (50)
Systemic hypertension
1 (50)
Pulmonary disease 0
Pulmonary embolism 0
Total
T. normal
50 to 69 Years
85
)}94
Downloaded from http://jcp.bmj.com/ on May 10, 2017 - Published by group.bmj.com
A simple method of weighing the heart
disease (normals) and there are no cases of pulmonary disease in either sex with L/R>3. The cases
of systemic hypertension are, however, rather widely
scattered. (2) T/R is 5 or more in 44 (22%) of
males and in 24 (25%) of females regarded as
'normal'; there is only one case of pulmonary
disease, a female. Again systemic hypertension is
quite widely distributed. (3) D (L/R-T/L), in which
a value of 0 or less includes 48 (87-5 %) cases of
pulmonary disease in males and 19 (90%) cases
in females. In systemic hypertension (which takes
precedence when both conditions are present) 5 %
and 2 % respectively fall in this range and in normals
the incidence for the two sexes is 1 % and 12%.
583
In order to examine further the variability of these
three series and of the total heart weights probability
curves were constructed using a log. normal scale
except in the case of D where there are negative
values (Figs. 8 to 11). In each case the 95% range
(2-5 % to 97-5 %) is shown and the median can be
derived from them for each category. These curves
indicate clearly the variability of each series and very
approximate significance tests are shown in Table
II. The only occasions when there is no apparent
significant variation concern the curves for 'all cases'
in T/R and D. It seems reasonable to suppose therefore that the variations in the heart weights in L/R,
T/R, and D in the various categories are distinct
TABLE II
No. of Cases
ANALYSIS OF FIGURES 8 TO 11
Median
95 % Range
a (Approximately)
Difference of
S.E. of Difference
Median from
Median of Normal
Heart Weight
Maks
Normal
Systemic hypertension
Pulmonary diseases
All cases
195
179
55
429
325
430
216-495=244
425
435
255-565=310
235-600=365
274
375
345
325
195-495=300
255-570=315
205-545=340
75
79
150-600=450
113
315-655-340
61
85
78
91
-
-
105
+ 7-7
100
110
±11-4
± 6-2
Females
Normal
Systemic hypertension
Pulmonary diseases
All cases
107
93
21
221
85
-
101
71
51
±10-9
±19-9
±100
LIR
Males
Normal
Systemic hypertension
Pulmonary diseases
All cases
195
179
55
429
2-37
2-8
1-65
2 45
1.63-3-4=1-77
1-63-4-7=3 07
10-2-33=1-33
1-38-4-0=2-62
0 44
0-77
0-33
0 65
Females
Normal
Systemic hypertension
Pulmonary diseases
All cases
107
93
21
221
2-35
2-85
1-78
2-35
1-6 -3-55= 1-95
0-49
0-81
0-3
0-73
-
-
1-3 -2 5 =1-2
1-48-4-4 =2-92
0-5
057
0
±0-1
±0-08
4-38
4-9
3-4
3-08-6-05=2-97
0-74
-
Pulmonary diseases
All cases
195
179
55
429
3-3 -7-5 =4-2
2-53-4-45 = 1-92
2-9 -6-8 =3-9
105
0-48
0-98
052
0-98
0-12
Females
Normal
Systemic hypertension
Pulmonary diseases
All cases
107
93
21
221
4-4
3-25-5-75=2-5
3-4 -8-0 =4-6
2-4 -5-1 =2-7
3-0 -6-3 =3-3
0-63
0-68
0-83
0-5
0-8
0
195
+0-7
+ 1-1
-0-4
+0-7
-04-+ 1-75=2-15
-05-+2-7 =3-2
-1-45-+0-6 =2-05
-0-85- +2-25=3-1
054
0-8
0-51
0-78
0-4
1-1
0
+0-5
-0-85- ±1-95=2-8
-0-3 -+3-45=3-75
-1-35-+0-3 =1-65
-0-7 -+2-65=3-35
0-7
0-94
0-41
0-84
-
-
0-5
0-75
±0-12
±0-11
TIR
Maks
Normal
Systemic hypertension
4-5
4-9
3-6
4-4
1-73-4-95=3-22
1-15
-
0-43
0-72
0-08
-
-
±0-07
±0-06
±0-03
-
-
±0-095
±0-084
±0-071 NS
-
±0-13
±0-16
-
D
Males
Normal
Systemic hypertension
Pulmonary diseases
All cases
Females
Normal
Systemic hypertension
Pulmonary diseases
All cases
179
55
429
107
93
21
221
+1-0
-0-25
+0-6
-
01
-
±0-07
±0-08
-
±0-09 NS
Downloaded from http://jcp.bmj.com/ on May 10, 2017 - Published by group.bmj.com
A. G. Maishall
584
U
Cn
N
0
N
CO
z
0
CZ 6
I)
W)z
I. N
<
4
C
w
CO
4
CaQ
o E <
>1
jn
I
C
er
tn
z-<UO
Lll...
D
4
>-O
aCZ
C
IN
QOE
B
iN
N
I
a
-
C en4a0
.0
N
N
C
4
=
am 4
i-
,~
b
0
0W
4
(4
0
0t
en
en
4
en
en
.
a
I
0
Cr
lf~
b
EM T
06
U)
s0
N
CO
UO
6t
C)
9
.N
0
en
LI)
0
C
Lx
cx
1C
N
'I
N
co
N
cN
CI
NO0
-
S3SVD J10 b3SvfnN
CO
0
C
N
,,
.
C
a
0N 04
,I ,, ,
N
0
O)
04
.
I
CO
C
-
NO
-
-
-J
. .
CO
-
S3SV2) Jo U3NfnN
t
N
Downloaded from http://jcp.bmj.com/ on May 10, 2017 - Published by group.bmj.com
A simple methol
of
585
weighing the heart
tU)
ol
iv
z
<
N
CY
F
S
(f
-
0
a Q.w
x
14
0
LW4\'='NlI
L-
2
<
>.0
10
N
O.
I1N
:~~~~ N
-
In
It
0
-
b~
~~~
~~~~
~~~
~~~~
~~~
~~~
~~~
~~~
~~~
~~~
~~~
~~~
~~~
~~~
N
N
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
o
1D
oS
.~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~.
UN
'I~~~~~~~~~~~~~~~~~~~~~~~~~
14)
FAEAFFWNIrIffl-MIZIM
C
0
CV
en
I
T
M
Ir
Sn
IV)
=
2
0
an
NM
~
~
.
.
.
W
X
S
.
A,
0
_4
ix
-i
-J
N
S3SYD
U083Gv4lN
4- 50
-
b
t
S3SV) ziO b3smnN
N
-
Downloaded from http://jcp.bmj.com/ on May 10, 2017 - Published by group.bmj.com
A. G. Marshall
586
u}
U)
.
I?)
N
0
In)
_
z
0
#)
0
o
oW
z
w
0
0
lb
4c
J
-
T
I
0
z
40
0
fU'0
IV
4l
ub
U)Z
0.
o4~ ~ ~4
-
a
-i
*
r-
|uW
V
I
XI
V
Mv)we
"I'4i
m
v
r'0
7
4
9
lb
4q
I
as
lb
th
'0
'0
14
o
sl)
la
b
o
U0
Ce)
I
'0
I
C,)
40
'0
TIt
0
U)
4p
in
N
e1
-0
I
N
in
I
lp
In
lp
N
ar
.
sO
U)
4(
;
N
-o
S
-
OW
0
rN aO
U)
O;i39VOflN
S3SV:) :0 ?33gvnN
4
N
-
I
.
.
.
.
_~~~
a
.
.
;
0
.
.
_
S3SV:) JO b3gymN
.
.
.
.
.
N
-
Downloaded from http://jcp.bmj.com/ on May 10, 2017 - Published by group.bmj.com
A simple method of weighing the heart
587
0
In
Oh
in
I.
0l
z
0
a
In
W I-
ILz
I
0
-w
QoM.
m1
In
In
0
14
OUI
In
N.
z
I')
U
~~i:
mm
I
m
qw
qo
1*
F'
'0
k-
4i
'0
0
to
4cp
'0
SI
lb
lb
Io
SI
In
'0
b
t0
%-.a
in
In~
la
'If
SIZ
'0
b
9'0
=
SI
'Ib
Olh
r = In
b0
-0SSI.
I.
'0
"4
=
'p
In
'0
1.
'2
In
"4
IL
0
A
n
a
n
Oh
G0
N
'0
s3s D)
a
We
a
0
EQ
Ncm
I0
Oh
0
N
le
ti3gvqANSs3sv:)
In
le
EQ)
:jo ti3sy4nN
EC4
Downloaded from http://jcp.bmj.com/ on May 10, 2017 - Published by group.bmj.com
A. G. Marshall
588
I
0
0
6
A
.8
z
0
w U)
Ln z
L-1
_I---
L-1
4
0
8
w
0.
op
0
u
I
z
1
Sn
Ul)
4
4t
0
0
=
w
4
0
z
.q
0
0.
N
0UU
0
Ul)
m o.
S.)
19
0
m
N
m
Sq
0
0
m N
(9
0
'0
1o
N
=
v
N
A
*1
'p
'a
b
I
S.)
'0
1
V~.
0
1o
zo
N
=
N
:
=~
ID
N
N
r0
N
N
1o
9
I
0
0
'a
=~
0
b.
'0
0
IL
*5
=-
0
F.Sn
0
N
'a
F
'a
0
co
F'.
F.,
IEn
0
N
I -
0
v
0c0
.
.
'.'0
9
Sn
.
*-
.
9
N
a
0
.
-0 0s
6
-0
5
.
F''0
S3SV:) 10 U39rinN
9
Sn
v
0
V M.
-
0 0 F 0 Sn't")N -000
r'
S3SV: i0 13gvmN
l N
-
Downloaded from http://jcp.bmj.com/ on May 10, 2017 - Published by group.bmj.com
589
A simple method of weighing the heart
mm
wtwtt* o
OD
k
ic;
C,)
o~ ~ ~ ~ ~ ~ ~ ~ ~ -
-
z
0
'p
0
wU
1
c,)
Z
Lt
<
~nUV)
10
Ca
It
I
>-
Ix
10
Z
1.
C,)
T
-
-J
C,)
_O
c,r)
0*
af
O.
0
en
z
(f
z
0
C,)
Cll
0
C,)
0
N
I
I-%'7
M..
b
b
0
to
0S
C
I?
I
.M 0
o
N
C;'
o0
Cl
0
!0
-
MWI.
I
T
Cli
0
r.0
U.
co1
to
N
6
1
IL
0
(,)
0
0
1
I
I'
t)
Cl
T
NC
Ui
enC:
I
I
Cq
cF
N
b o
S3SVD
u)
t
fl0 b3
I'
-
b
g
;
w
(r
S3SVO 30 U39rwnN
NSAnN
I
...
Downloaded from http://jcp.bmj.com/ on May 10, 2017 - Published by group.bmj.com
590
A. G. Marshall
HEART WEIGHT (MALE)
.-I
k-
% OF
CASES
97.5
90
70
50
30
10
2-5
I
I
F. a200
8a
Io.
IHEART
I
250
I
I
-
300
CASES
LIR (MALES)
I g1A
I
I
I
I
I
I
I
I
I Ia
I
a
r
70
50
10
2*5
I
I
05
iII
I
1-5
1
I
I I
I
I111
2 25 3354455
FIG. 9a
WEIGHT (G)
I
I
97-5i
550 650
450
I
OF
CASES
* II
I
350
HEART WEKIT (FEMALES)
I
I
I
% OF
I
LIR (FEMALES)
I
A
a
I
I
I
I
lIaI I
7 OF
CASES
97.5
90
70
50
30
10
2-5
I
FIG.
8b
20O
I
250
I
300
I
I
400
I
I
1
T5
I
FIG.
50
9b
1. 0
15
20
.
.
I.
I
I
20
3
4550
40*
HEART WEI3HT (G)
*~~*
=
all cases,
o-o
=
normals,
x
x
=
8a and b. Percentage of cases found below each
value of heart weight in each category (adults).
FIGS.
systemic hypertension, Ak--A
nGS. 9a and b.
Percentage of
=
pulmonary disease
cases
value ofLIR in each category (adults).
found below each
Downloaded from http://jcp.bmj.com/ on May 10, 2017 - Published by group.bmj.com
A simple method of weighing the heart
TIR (MALE)
a
(MALES)
D
I
a£
I
A-I
A
11J
I
591
I
a
a
II
II
aI
I0
a
i
7. OF
CASE S
7 OF
CASES
_
'97.5_
97.5
0
90
70
50
50
30
30
10
10
2-S
r
FIG. IOa
2-5
*
I
I
I
3
35
4
I
1
* Iu
46 5 586667
L
I
FIG.lla
-2
TIR (FEMALES)
a
D
I
I
I
A.
I
2
1
3
4
5
(FEMALES)
I
. OF
CASES
*
OF
CASES
97.5
5"
97.-
90
90
70
70
50
50
30
30
10
10
2-5S
A
I
2-5
I
I
3
I
3.5
I
4
I
I
I
I
45 55886 7
FIG. l Ob
*
FIG.
*
=
all cases,
o-o
=
normals, x
x
=
-2
-1
systemic hypertension,
10a and b. Percentage of cases found below each
value of TIR in each category (adults).
FIGS.
llb
A
2
1
0
-
=
I
I
I
3
4
5
I
pulmonary disease
1lla and b. Percentage of cases found below each
value of D (LIR-TIL) in each category (adults).
FIGS.
Downloaded from http://jcp.bmj.com/ on May 10, 2017 - Published by group.bmj.com
592
A. G. Marshall
and may be associated with the interpretations
which we have put on them. Although these calculations are approximate, there seems no reason to
suppose that more laborious and exact methods
would lead to different conclusions.
Pulmonary embolism This is acute massive
embolism usually post-operative or post-traumatic.
There are 17 cases in the 120 with reversed ratios
and 29 with normal or raised ratios. This difference
being significant at the 1 in 1,000 level suggests that
acute pulmonary embolism is associated with pulmonary hypertension and the two are bracketed in
the final column of Table I.
If the figures in Table I are re-tabulated ignoring
the total weight of the heart, much of their significance is lost, especially when the ratios are normal
but less so when the ratios are raised or reversed.
Perhaps this is due to including more cases of
'uniform hypertrophy' among the normals, but it
destroys our hope that use of the fractions would
entirely remove the difficulty of defining the weight
of the normal heart.
HEART WEIGHT ANALYSIS ACCORDING TO DISEASE
Three diseases of the pulmonary system were extracted from Table I in order to determine if it is
legitimate to include them in a category which is so
suggestive of pulmonary hypertension.
Pulmonary tuberculosis There are seven cases in
the 120 with reversed ratios and six cases in the 530
of normal or raised ratios. This difference is significant at the 1 in 1,000 level so that it seems justified
to leave them as they stand in Table I.
Carcinoma of lung In the 120 cases with reversed
ratios there are 10 cases of carcinoma of lung or
bronchus and 25 in the 530 cases in the other groups.
These differences are significant only at the 1 in 10
level and it is concluded that this disease is not
associated with pulmonary hypertension. This
material was therefore withdrawn from the pulmonary group and re-allocated to other categories;
the new totals are shown in the final columns of
Table I and these figures have been used in the other
analyses.
HEART WEIGHTS IN ADOLESCENTS, CHILDREN, AND
INFANTS An arbitrary division of this material into
these three groups has been mentioned previously.
Difficulty in deciding the normal heart weight in these
cases (Sunderman and Boerner, 1949), lack of recorded blood pressure readings in almost all cases,
and the small numbers prevent any valid analysis,
especially in the first two groups. The findings in
adolescents and children are shown in Table III
,LE III
RESULTS IN ADOLESCENTS AND CHILDREN
Male
Female
10 to 19 Years
No.
Age
of
Cases
Ratios
17
19
Ratios
raised
4
10 to 19 Years
No.
Age
of
Cases
10
13
13
16
16
normal
I to 9 Years
No.
10
12
14
16
HW 95
HW 260 Leukaemia
HW 230 Appendicitis
HW 315 Bronchiectasis
HW 235
HW 290 Bronchiectasis
HW 280 Accident
Drowned, no details
Accident, no details
Cerebral haemorrhage
B.P. 150/70 mm. Hg.,
1 to 9 Years
No. Age
of
Cases
Age
ofi
Cases
6
No comment
2i HW 70 Leukaemia
3
3
unconscious
5
Rheumatic carditis
6
HW 60 Leukaemia
HW 85 Miliary tuberculosis
HW 85 Brain tumour
HW 220 Coronary
thrombosis.
No B.P. read-
5
1
6
14
15
13j
HW 155 Bronchiectasis
HW 195
HW 235
HW 240
HW 255
15
HW 215 Tuberculous
3
11
13
No comment
2i
HW 55 Septicaemia,
54
lung abscess,
congenital abnormal kidneys
HW 130 B.P. 150/100
mm. Hg
HW 130 Septicaemia,
meningitis
6
adrenal haemorrhage. No
ing
B.P. reading
Ratios
reversed
2
10
14
Mitral stenosis
Collapse, cor pulmonale
6
Rheumatic carditis
HW 100
3
2i HW 80 Congenital
heart disease
31
5
HW 85 Fallot's
tetralogy
HW 100 Fibrocystic
disease of pancreas and bronchiectasis
HW
=
Heart weight in
grams
Downloaded from http://jcp.bmj.com/ on May 10, 2017 - Published by group.bmj.com
A simple method of weighing the heart
593
TABLE IV
RESULTS IN INFANTS
Male
Female
No. of Cases
Ratios
normal
18
Ratios
raised
9
Ratios
reversed
31
No. of Cases
All ages j hr. to I year, premature and stillbirth
Two congenital heart disease, 3 days and 1 month
One abnormal kidneys and ureters, 9 days
No cases of hydrocephalus
Two with abnormal kidneys and ureters, stillbirth and
six weeks
Two hydrocephalus, 4 months and 20 months
Ratios equal (L/R =T/L) in six, 2 days to 2 months
Two congenital disease of heart, I week to 6 weeks
23 all under 5 days except two at 14 and 12 days premature, one at 10 days no history, one at 26 days, hydrocephalus
and it will be seen that there is some suggestion that
they are similar to those in adults. Two boys and
one girl with normal ratios had bronchiectasis and
it is probable that pulmonary hypertension with
right ventricular hypertrophy had not yet become
established at this age. Attention is drawn to the
interesting possibility of systemic hypertension in
two boys aged 14 and 6 years with raised ratios
and also in two girls aged 5j and 24, the latter with
renal disease. It will be further noted that two of the
four cases with reversed ratios would be expected
to have pulmonary hypertension.
The findings in 95 necropsies on infants are shown
in Table IV and they suggest that the ratios, which
are usually reversed at birth (as would be expected),
begin to conform to the adult pattern at about a
week or soon afterwards. Some possible reasons for
a departure from this rule are also shown in Table IV.
The final conclusions may be re-stated simply:
(1) When L/R.3 and/or T/R.5, there is left
ventricular hypertrophy which, other causes being
excluded, is suggestive of systemic hypertension.
This association is enhanced if the weight of the
heart is increased. (2) When L/R-T/L (D) is 0 or
less, other causes being excluded, there is strong
evidence of pulmonary hypertension. This association is largely independent of total heart weight and
such values are unlikely to be found in the presence
of cardiac hypertrophy consequent on systemic
hypertension. Conversely it is most unlikely that
pulmonary hypertension is present when L/R.3
and/or T/R>5.
DISCUSSION
It is important to stress that these figures can only
be regarded as useful when they are considered with
the whole of the clinical and post-mortem findings.
In these circumstances a departure from normal
ratios, whatever the weight of the heart, requires
3
11
2
24
All ages still birth to 5 weeks and premature
One case hydrocephalus
One intussusception, 11 weeks
One hydrocephalus and spina bifida 10 weeks
Two congenital disease of heart
21 ali under 5 days except one at 5 days hydrocephalus
explanation and the method has therefore some value
which is enhanced by its simplicity.
In the past, especially when there was no record
of the blood pressure or when such a record might
be regarded as unreliable owing to the clinical
deterioration of the subject, there has been a tendency to consider an increased heart weight suggestive of systemic hypertension, other explanations
being lacking. This new technique has to some
extent defined more clearly the criteria on which such
a conclusion could be sustained and has revealed a
method by which pulmonary hypertension can be
diagnosed after death.
The finding that acute pulmonary embolism is
associated with pulmonary hypertension emphasizes
the risk of post-operative and post-traumatic immobilization in patients with chronic pulmonary
disease. Such people may be considered as especially
suitable for early prophylactic anticoagulant therapy.
Their extra susceptibility to this complication is
presumably due to venous stasis consequent on the
pulmonary hypertension and of course the added
risk to such individuals is not confined to immobilization in hospital but is also present when they are
confined to bed at home. Phear (1960), in a followup study of patients surviving pulmonary embolism,
found that nearly 15% were severely disabled by
pulmonary hypertension. It seems from our own
findings that this condition was probably present
before the embolic episode which in these severely
disabled survivors may have accentuated it.
These results were compared with those published
in detail by Lewis (1914) and by Herrmann and
Wilson (1922) by calculating the ratios L/R, T/R,
and T/L from their figures after adding the weight of
the septum to their left ventricular weight. In the
latter case, although the septum was divided, a
reasonably good correlation was found with these
conclusions, but in Lewis's tables no such correlation
could be found. Herrmann and Wilson remark that
Downloaded from http://jcp.bmj.com/ on May 10, 2017 - Published by group.bmj.com
594
A. G. Marshall
Lewis's method is inaccurate to the extent of 18 g.
lost on one ventricle and calculations from his
figures show that they deviate from these, chiefly in
the ratios T/R and T/L.
It seems that the value of this method is enhanced
by its applicability to either sex at any age and its
apparent validity in children and infants should be
of special interest.
Jacobs, Dr. C. B. Whittaker, Dr. B. Godwin, Dr. H. G.
Alton, Dr. Hameed.
I wish to acknowledge my gratitude to Professor J. R.
Squire and members of his staff for their help with the
statistical analyses and for some of the figures.
Dr. Avril Oatway has given much help both with
necropsies and tabulating results. Other pathologists who
performed necropsies are Dr. Martin Israel, Dr. Allan
Bartels, E. C., and Smith, H. L. (1932). Amer. J. med. Sci., 184, 452.
Heath, D., and Whitaker, W. (1955). J. Path. Bact., 70, 285.
Herrmann, G. R., and Wilson, F. N. (1922). Heart, 9, 91.
Lewis, T. (1914). Ibid, 5, 367.
Phear, D. (1960). Lancet, 2, 832.
Sunderman, F. W., and Boerner, F. (1949). Normal Values in Clinical
Medicine. Saunders, Philadelphia and London.
Zeek, P. M. (1942). Arch. Path. (Chicago), 34, 820.
Mr. H. J. Flewitt weighed and recorded all the material
and we express our special thanks to him.
I wish also to thank Mr. A. Hemsley for drawing
Figs. 4-7 inclusive, and Mr. R. Paton and Mrs. R. Harpin
for the photographs.
REFERENCES
The September 1961 Issue
THE SEPTEMBER 1961 ISSUE CONTAINS THE FOLLOWING PAPERS
The artificial kidney and urea clearance D. J. BLACKMORE Antistreptolysin levels in normal infants and young
and w. J. ELDER
children c. w. POrrER and J. LORBER
A new principle applied to the determination of calcium Fatal septicaemia due to Salmonella cholerae suis I. s.
in biological materials by flame photometry J. K. BAILEY, G. GARRETT, and A. NICOL
FAWCETT and v. WYNN
Serum precipitin reactions in Hashimoto's thyroiditis
Estimation of gamma globulin in the serum of patients J. M. MOORE
with hypogammaglobulinaemia R. A. KEKWICK, L.
Minimal criteria for the diagnosis of megaloblastic
VALLET, M. CUTBUSH, P. L. MOLLISON, A. R. THOMAS,
anaemia
of pregnancy I. RANNIE and H. MCTAGGART
P. G. H. GELL, and J. F. SOOTHILL
factor deficiency, capillary defect of
Antihaemophilic
The antithrombin activity of glucuronic esters of bilirubin M. KOPEC, T. DAROCHA, S. NIEWIAROWSKI, and von Willebrand type, and idiopathic thrombocytopenia
occurring in one family E. K. BLACKBURN, J. M. MACFIE,
J. STACHURSKA
Studies on the disturbance of glucuronide formation in J. H. MONAGHAN, and A. P. M. PAGE
infectious hepatitis M. F. VEST and E. FRITZ
Coagulation tests on capillary blood KATHARINE M.
Rapid incremental methods for the determination of DORMANDY and R. M. HARDISTY
serum iron and iron-binding capacity R. N. BEALE, The anaemia of lead poisoning H. E. HUTCHISON and
J. 0. BOSTROM, and R. F. TAYLOR
J. M. STARK
Lipids in cadaver sera after fatal heart attacks J. B.
The recognition of Hageman deficiency in blood donors
ENTICKNAP
W. L. MARSH and J. JENKINS
Serum alkaline phosphatase fractionation as an aid to
diagnosis K. B. COOKE and JOAN F. ZILVA
The determination of 3-methoxy 4-hydroxy mandelic acid
in urine. A. J. WOIWOD and R. KNIGHT
Factors concerned in the efficient steam sterilization of
surgical dressings R. J. FALLON
A case of meningitis due to Listeria monocytogenes
Renal enlargement in chronic cor pulmonale P. A. ELLIS
Technical methods
A contact slide method for the isolation of staphylococci
I. A. PORTER and JOYCE NICHOLSON
A micro-method for measuring glucose using the Autoanalyzer and glucose-oxidase CYNTHIA WINCEY and
A. BECK
VINCENT MARKS
Disinfection of woollen blankets in steam at subatmospheric pressure v. G. ALDER and w. A. GILLESPIE
Nasal abnormality and the carrier rate of Staphylococcus
A micro technique for protein concentration suitable
for quantitative electrophoresis of cerebrospinal fluid
aureus
J. COLOVER
s. I. JACOBS, G. M. WILLIAMSON, and A. T. WILLIS
The iron method of haemoglobin estimation J. FINE
A contribution to the technique of intracutaneous testing with toxoplasmin oTTo JIROVEC and JINDAICH JfRA Book reviews
Copies are still available and may be obtained from the PUBLISHING MANAGER,
BRMSH MEDICAL ASSOCIATION, TAVISTOCK SQUARE, w.c.l, price 17s. 6D.
Downloaded from http://jcp.bmj.com/ on May 10, 2017 - Published by group.bmj.com
A simple method of weighing the
heart
A. G. Marshall
J Clin Pathol 1961 14: 578-594
doi: 10.1136/jcp.14.6.578
Updated information and services can be found at:
http://jcp.bmj.com/content/14/6/578
These include:
Email alerting
service
Receive free email alerts when new articles cite this
article. Sign up in the box at the top right corner of
the online article.
Notes
To request permissions go to:
http://group.bmj.com/group/rights-licensing/permissions
To order reprints go to:
http://journals.bmj.com/cgi/reprintform
To subscribe to BMJ go to:
http://group.bmj.com/subscribe/